Resistance to acute malarial infection with Plasmodium berghei yoelii (Pby) requires the presence of both T and B lymphocytes as determined in studies utilizing athymic nude mice and mice rendered B cell deficient by treatment with anti u chain serum. Furthermore, acute malarial infection does not constitute an immunizing event in effected nude mice. When parasitemias in these animals are arrested with clindamycin, malaria recurs. B cell deficient chickens are similarly susceptible to the lethal effects of acute malarial infection, but they develop "nonsterilizing immunity" which prevents recurrent disease and allows them to resist challenge. We will now determine if B cell deficient mice behave in a similar manner following drug treatment of acute malaria. Since increased splenic cellularity and activation of the RES are associated with resolving malarial infections, we will determine if these parameters of immunity are T cell dependent. This will be accomplished by measuring splenomegaly and carbon clearance in mice lacking T.B. or both types of immunocytes following drug treatment of acute infection with Pby.